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STROKE

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Sidar Aydin

on 11 November 2015

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Transcript of STROKE

STROKE
Sidar Aydın
History & Definition

STROKE
Epidemiology of the Disease
Classification of the Causes
of the Disease

Blood Supply to The Brain
Treatment
Discussion
(A)etiopatogenesis & Pathophsyiology
of Ischemia
Rapidly developing clinical signs of focal or global disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin.
STROKE

Hippocrates
Johann Jakob Wepfer
Apoplexy
Struck down by violence.
Bleeding in the brain.
Blockage in one of the brain's blood
vessels could cause apoplexy.
Cerebral Vascular Accident
(CVA)
Apoplexy
Blood in the Brain
STROKE
Brain Attack
STROKE
Ischemic Stroke
Hemorrhagic Stroke
* Thrombosis
* Embolism
* Global loss of blood flow



(Systemic hypoperfusion)
85%
15%
* Intracerebral
* Subarachnoid
BLOOD SUPPLY TO THE BRAIN
?
Large Vessel Thrombosis
(Macroangiopathy)
Small Vessel Thrombosis
(Microangiopathy)
Thrombosis
Local obstruction of artery due to degenerative changes in arterial wall.
Large Arteries (Macroangiopathy)
Small Arteries (Microangiopathy)
Large Arteries (Macroangiopathy)
- Territorial Infarctions
- Borderzone Type Infarctions
- *Watershed Type Infarctions
- Lacunar Infarctions

* Infarct: Localization of dead tissue
Territorial Infarctions
Large Arteries (Macroangiopathy)
Borderzone Infarctions & Watershed Infarctions
* Total Anterior Circulation Infarct(TACI)
* Partial Anterior Circulation Infarct(PACI)
* Posterior Circulation Infarct(POCI)
* *Lacunar Infarct(LACI)
[Oxford Stroke Classification]
Small Arteries (Microangiopathy)
Lacunar Infarctions
Lacunar infarcts are small deep infarcts in the distal distribution of penetrating vessels (lenticulostriate, thalamoperforating, pontine perforating arteries, recurrent artery of Heubner)
Territorial infarcts are large infarcts, occur at cerebral vascular territories.
Bordezone and watershed infarcts occur at the border between cerebral vascular territories.
Embolism
An embolus is any detached, traveling intravascular mass carried by circulation, which is capable of create an arterial occlusion at a site distant from its point of origin.
Emboli generally form as blood cloths but it also can form from air bubbles, fat globules, or plaque from an artery wall. Emboli can also result from abnormal heartbeat (atrial fibrillation), a condition in which the heart doesn’t beat effectively, causing blood to pool and clot.
Global Loss Of Blood Flow (Systemic Hypoperfusion)
Profound reduction in systemic blood pressure due to any reason is responsible for “hypotensive stroke.”

Global ischemia causes the greatest damage to “boundary zone” or “watershed area.” The parietal-temporal-occipital triangle at the junction of the anterior, middle, and posterior cerebral arteries is most commonly affected. Watershed infarction in this area causes a clinical syndrome consisting of paralysis and sensory loss predominantly.
Pathophysiology of Ischemia
1. Basal Metabolism of The Brain
Cerebral Blood Flow(CBF) - 50‐- 70 ml / 100 g / min
Cerebral Metabolic Rate of Oxygen(CMRO2) - 3.5‐ml / 100 g / min
Cerebral Metabolic Rate of Glucose(CMRGluc) - 33 μmol / 100 g / min
Hemorrhagic Stroke
2. Mechanisms of Neuronal Injury
Ischemic cascade
Ischemic Cascade
Anaerobic Metabolism
Lactate & Hydrogen Ions
Steps Until Complete Stroke
Asymptomatic Stenosis
Transient Ischemic Attack(TIA)
Reversible Ischemic Neurologic Deficit(RIND)
Progressive Stroke
Complete Stroke
CBF: 20 - 30 ml/100 g/min = Loss of Electrical Activity (Functional Threshold)
CBF: 10 ml/ 100 g/min = Neuronal Death (Morphological Threshold)
Low Oxygen & Glucose
Lack of Energy
Na+/K+ ATPase Pump Impairment
Anoxic Depolarization
Increase of Extracellular K+, Intracellular Na+ and Ca2+
Pannexin Channels ->
Extracellular ATP increase
Vesicular Glutamate Release
Post-synaptic NMDA, AMPA, Kainat Receptors Overexcitation
Accumulutaion of Ca2+ in Postsynaptic Neuron
Vesicular Glutamate Release
Disruption of the integrity of outer mitochondrial membrane, enabling the release of cytochrome c and other apoptogenic factors.
Apoptosome
Procaspase 9
Caspase 9
Apoptosis
Caspase 3
Cytochrome c + dATP
Calcium-Calmodulin
Neuronal Nitric Oxide Synthase
(nNOS)
L-Arginine
Nitric Oxide(NO)
*Free radical NO, Peroxynitrite
Oxidative Damage of Cellular DNA, Lipid Peroxidation, Excitotoxic Cell Death
Formation of Superoxides
Reactive Oxygen Species(ROS)
Activation of Phospholipase A2
Membrane
Phospholipids
Arachidonic Acid
COX
Prostoglandins
Lipoxygenase
Leukotriens
Acidosis
Necrosis
NMDA Ch. Opening
Prostoglandin G
Prostoglandin H +
•O2 -
Stroke Treatments
Ischemic Stroke Treatments
Hemorrhagic Stroke Treatments
Drug Treatment
Endovascular Procedures
*Anticoagulants
-> Prevent the coagulation of blood
+Warfarin (Coumadin), Heparin
+Dabigatran, Apixaban, Rivaroxaban
* Antiplatellets(Antiaggregants)
-> Decrease platelet agregation, thus,
inhibit thrombus formation.
+Aspirin, Clopidogrel, Dipyridamole,
Ticlopidine
*Tissue Plasminogen Activator(TPA)/ Recombinant TPA
* Catheter Insertion & Clot Dissolving
Epidemiology
Data of 2012 shows that the age-standardised stroke-mortality rates in
Fr
an
ce
are 24–38, in
Ger
ma
ny
37–47, in
It
a
ly
41–68, in
S
pai
n
38–52, in
U
.
K
.
46–53 and in

U
.
S
.

32–35 deaths per 100 000 persons per year.

1 in every 10 deaths
It is the third most common cause
of death in developed countries,
exceeded only by coronary heart
disease and cancer.
Worldwide, has one of the highest rates of mortality (19.9% of all deaths in China), along with Africa and parts of South America.
CHI
NA
Countries in

Eastern European
region register high stroke death rates.
The highest rate of 249/100 000 was noted in
Bu
lg
aria
, and the lowest of 27/100 000 in
Swi
tzer
land
.
Prevalance
Epidemiology
Incidance
• 795,000 new or recurrent strokes occur per year in the US, accounting for approximately 1 in 18 deaths
• Worldwide, people suffer a stroke
each year
; one-third die and one-third are left permanently disabled.
15 Million
Mortality
• Between
20-30%
References
* Stroke, 5th Edition. Pathophysiology, Diagnosis, and Management By J. P. Mohr, MS, MD; Philip A. Wolf, MD; James C
http://www.who.int/healthinfo/statistics/bod_cerebrovasculardiseasestroke.pdf
* The Atlas of heart disease and stroke, WHO 2004. http://www.who.int/cardiovascular_diseases/en/cvd_atlas_15_burden_stroke.pdf (Mackay J, Mensah G: The Atlas of Heart Disease and Stroke. Geneva, Switzerland, World Health Organization, 2004)
* Roger et al. AHA Heart Disease and Stroke Statistics 2011 update: a report from the American Heart Association.Circulation 2011;123:e18-e209.
* Sousa RM, Ferri CP, Acosta D, et al. Contribution of chronic diseases to disability in elderly people in countries with low and middle incomes: a 10/66 Dementia Research Group population-based survey. Lancet 2009;374:1821-1830.
* Kim AS & Johnston SC. Global variation in the relative burden of stroke and ischaemic heart disease. Circulation 2011;124:314-323.
* ZHANG Y, CHAPMAN A M, PLESTED M, JACKSON D, PURROY F 2012 The incidence, prevalence, and mortality of stroke in France, Germany, Italy, Spain, the UK and US: A literature Review.Hindawi Publishing Corporation. Stroke Research and Treatment
* EROS Investigators. Incidence of stroke in Europe at the beginning of the 21st century. Stroke 2009;40:1557-1563.
* Ingall T. J Insur Med. 2004;36(2):143-52.Stroke; incidence, mortality, morbidity and risk.
* http://www.nebraskamed.com/health-library/232034/history-of-stroke
* http://www.strokecenter.org/professionals/brain-anatomy/blood-vessels-of-the-brain/
* Uston, Cagatay (February 20, 2004). "Dr. Thomas Willis' Famous Eponym: The Circle of Willis". Turkish Journal of Medical Sciences 34: 271–274. Retrieved 16 July 2010
Boorder, Michiel J.; Van Der Grond, J; Van Dongen, AJ; Klijn, CJ; Jaap Kappelle, L; Van Rijk, PP; Hendrikse, J (2006). "Spect measurements of regional cerebral perfusion andcarbon dioxide reactivity: Correlation with cerebral collaterals in internal carotid artery occlusive disease". J Neurol 253 (10): 1285–1291.
* Merck & Co. Occlusive Peripheral Arterial Disease, The Merck Manual Home Health Handbook website, revised and updated March 2010. Retrieved March 4, 2012.
Kumar V., Abbas A.K., Fausto N. Pathologic Basis of Disease
* Szydlowska K, Tymianski M: Calcium, ischemia and excitotoxicity, Cell Calcium 47:122–129, 2010.
* Higuchi M, Tomioka M, Takano J, et al: Distinct mechanistic roles of calpain and caspase activation in neurodegeneration as revealed in mice overexpressing their specific inhibitors, J Biol Chem 280:15229–15237, 2005.
* http://www.healthline.com/health-slideshow/embolic-stroke-symptoms#2
* https://www.uic.edu/com/ferne/pdf/pathophys0501.pdf
* http://www.ncbi.nlm.nih.gov/pubmed/8314918
* http://www.safar.pitt.edu/archive/content/grant/jc/2006/0616%20Jenkins.pdf
* http://www.istanbulsaglik.gov.tr/w/tez/pdf/noroloji/dr_huseyin_celebi.pdf
* http://www.strokeassociation.org/STROKEORG/AboutStroke/Treatment/Stroke-Treatments_UCM_310892_Article.jsp#
*http://www.strokeassociation.org/STROKEORG/LifeAfterStroke/HealthyLivingAfterStroke/ManagingMedicines/Anti-Clotting-Agents-Explained_UCM_310452_Article.jsp
Cerebral Vascular Accident
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